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Principal Investigator: Rukmini Govekar

Contact details

Office Phone: +912227405023

Laboratory Phone: +912227405000 extn 5345


Research Area

One Key Research Area: Proteomic and phosphoproteomic profiling of leukemic cells in chronic myeloid leukemia

Special interests: 1. BCR/ABL-mediated molecular alterations in myeloid and lymphoid leukemias. 2. Effect of neutrophilic proteases on tumor cells

About us: Our lab focuses on investigating the proteomic profiles of myeloid and lymphoid cells from BCR/ABL mediated leukemias. Aim is to identify molecules, which as markers or therapeutic targets can improve the current state of management of these leukemias. We are also investigating the effect of neutrophilic proteases on breast cancer cell lines which can enhance our understanding of the effect of tumor infiltrating inflammatory cells on behavior of tumor.



Effect of neutrophilic proteases on the membrane proteome and cellular characteristics of MCF-7 cells

Our previous studies on erythrocyte senescence in chronic myeloid leukemia identified serum cathepsin G-mediated cleavage of erythrocyte membrane protein band 3 as a potential mechanism for imparting senescent phenotype to the erythrocytes. This indicated that secreted neutrophilic proteases can have unforeseen effects in conditions associated with increased local or systemic concentration of neutrophils. We therefore wanted to understand the effect of cathepsin G secreted by tumor infiltrating neutrophils on tumor cells. We initiated studies to explore the role of cathepsin G in modulation of membrane proteome of breast epithelial cell line MCF7. Work done so far has revealed that the enzyme induces proliferation of MCF-7 cells. Membrane proteins cleaved by cathepsin G have been identified by 2D-MS approach. We would extend this in vitro study to understand the role of protease mileu at the site of neutrophilic infiltration in tumor and its effect on membrane proteome of tumor cells which can be then correlated with tumor behavior.

Proteomic and phosphoproteomic profiling of myeloid cells from patients with chronic myeloid leukemia

Chronic myeloid leukemia (CML) is associated with a specific chromosomal abnormality: the Philadelphia chromosome (Ph), originating from a reciprocal translocation between the long arms of chromosomes 9 and 22. This translocation produces the oncogenic fusion protein Bcr-Abl, with a constitutive tyrosine kinase activity with maintained autophosphorylation and substrate activation. The presence and activity of Bcr-Abl is necessary and sufficient to determine neoplastic transformation of hematopoietic multipotent cells. Specific drugs with anti-phosphotyrosine kinase activity especially, Imatinib mesylate, causes selective suppression of Bcr-Abl positive cell proliferation. Patients in chronic phase CML have a good response to imatinib (95% complete remission), but there are major obstacles to imatinib based therapies. One is the persistence of BCR-ABL-positive cells, known as the ‘minimal residual disease’, which requires necessitates continuous imatinib therapy for suppression of the disease. The other major problem is a refractory or loose clinical response because of innate or acquired resistance, caused by amplification of the BCR-ABL genomic locus or more frequently by point mutations within the kinase domain of BCR-ABL, which prevent imatinib binding. Moreover, patients in the acute phase of CML (blast crisis) do not respond to the tyrosine kinase inhibitors. In both CML-CP refractory to imatinib treatment due to innate or acquired resistance and in blast crisis, therapeutic targets other than BCR/ABL need to be identified. In the proposed study proteomic and phosphoproteomic analysis of mature and immature myeloid cells in circulation would be done to identify differentiator proteins and phosphoproteins. The data would provide the matrix for exploring potential therapeutic targets among the differentiators.


Laboratory Members:

Ms. Poonam Kawle, Scientific Assistant ‘D’

Ms. Mythreiyi Narsimhan, JRF

Mr Jayesh Tandel, Trainee

Ms. Prachee Sheth, Trainee


1. Charuta Murudkar, Pune University, Pune, May - June 1998

2. Rohit Varshney, Seth GS Medical College, Mumbai, May - June 2005

3. Renjan Thomas, Vellore Institute of Technology, Vellore, January- May 2006.

4. Naveen Ravi, Kempegowda Institute of Medical Sciences, Bangalore, July-September 2006

5. Pradymna Bharadwaj, BITS Pilani, Goa campus, May- July 2007

6. Veena Somasundaram, Dr. Mahalingam Center for Research and Development, Nallamuthu Gounder Mahalingam College (Autonomous) (Affiliated to Bharathiar University), Pollachi, January- March 2007

7. Sunitha Pullikot, VIT University, Vellore, December-June 2008

8. Pooja Mane, CKT college of Arts, Commerce and Science, Panvel, April 2009

9. Dipti Waghchoure, Jhunjhunwala College, Mumbai, February -May 2009.

10. Sheena PV, Karpagam Arts and Science college, Coimbatore, Dec 2008- March 2009

11. Gauri Hule, Birla College, Kalyan, May -August 2009; September 2010 to February 2011

12. Rupak Kumar, Bharathidasan University,Tiruchirappalli, July -October 2009

13. Saurabh Kudtarkar, DY Patil institute of biotechnology and bioinformatics, Belapur, January - June 2010

14. Clyde Pinto, Seth G.S. Medical College and KEM Hospital June - December 2010

15. Saurabh Satose, Ramniranjan Jhunjhunwala College, November 2010 - January 2011

16. Sarita Pillai, GN Khalsa college of Arts, Science and Commerce, Mumbai, May-August 2010

18. Ritika Vishwanathan, Banasthali University, Rajasthan, January - May 2011

19. Jasmine Bedi, VIT University, Vellore, Tamilnadu: May 2011 to July 2011

20. Amruta Uttarkar, Pillai College, New Panvel, July -October 2011

21. Mythreyi Narsimhan, VIT, Vellore , September 2011 - June 2012

22. Atul Pawar, BITS-Pilani, Hyderabad, June - July 2012

23. Sajda Khatoon, DY Patil University, Navi Mumbai, January - June 2012

24. Jayesh Tandel, August , 2012 –on-going

Opportunities: We will not be accepting a PhD student this year but would be willing to take motivated students to join for training.


Select Publications:

1. Govekar RB, Kawle PD, Advani SH, Zingde SM: Reduced PKC α Activity Induces Senescent Phenotype in Erythrocytes. Anemia. 2012;2012:168050. doi: 10.1155/2012/168050. Epub 2012 Sep 4. *corresponding author

2. Rukmini B. Govekar*, Poonam D. Kawle, Renjan Thomas R, Suresh H. Advani, Sheena P.V, Surekha M. Zingde Eryptotic phenotype in chronic myeloid leukemia: contribution of neutrophilic cathepsin G Anemia, vol. 2012, Article ID 659303, 7 pages, 2012. doi:10.1155/2012/659303 *corresponding author

3. Rukmini B. Govekar, Anil .K. D’Cruz, Kumar A. Pathak , Jaiprakash Agarwal, Ketayun A. Dinshaw, Roshan F.Chinoy, Nikhil Gadewal, Sadhana Kannan, Ravi Sirdeshmukh, Curam S.Sundaram, Siddhi A. Malgundkar, Surekha M.Zingde. Proteomic profiling of cancer of the gingivo buccal complex: Identification of markers for transformed epithelium and potential targets for therapy. Proteomics- Clin. Appl. 3: 1451–1462, 2009

4. R.B. Govekar and S.M. Zingde. Cancer proteomics: How far we are from the clinics? Invited review in Int J Human Genet. Special issue on Gene Expression Signature in Cancer 7(1), 91-97, 2007.

5. Govekar RB, Zingde SM.

Protein kinase C isoforms in human erythrocytes.

Ann Hematol. 2001 Sep;80(9):531-4.

Member:IACR, SBC

Contact Us

Advanced Centre for Treatment, Research and Education in Cancer

Kharghar, Navi Mumbai - 410 210, india

Phone:+91-22-2740 5000

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